UPDATE ON PREDICTION & PREVENTION OF PREECLAMPSIA

Assist. Prof. S. Rouholamin

HYPERTENSION IN PREGNANCY

Etiology & Definition

Complicates 10-20% of pregnancies

Elevation of BP ≥140 mmHg systolic and/or ≥90 mmHg diastolic, on two occasions at least 6 hours apart.

Categories

Chronic Hypertension Gestational Hypertension Preeclampsia Preeclampsia superimposed on

Chronic Hypertension

Chronic Hypertension

“Preexisting Hypertension” Definition

Systolic pressure ≥ 140 mmHg, diastolic pressure ≥90 mmHg, or both.

Presents before 20th week of pregnancy or persists longer then 12 weeks postpartum.

Causes Primary = “Essential Hypertension” Secondary = Result of other medical

condition (ie: renal disease)

Prenatal Care for Chronic Hypertensives Electrocardiogram should be obtained in

women with long-standing hypertension. Baseline laboratory tests

Urinalysis, urine culture, and serum creatinine, glucose, and electrolytes

Tests will rule out renal disease, and identify comorbidities such as diabetes mellitus.

Women with proteinuria on a urine dipstick should have a quantitative test for urine protein.

Treatment for Chronic Hypertension Avoid treatment in women with

uncomplicated mild essential HTN as blood pressure may decrease as pregnancy progresses.

May taper or discontinue meds for women with blood pressures less than 120/80 in 1st trimester.

Reinstitute or initiate therapy for persistent diastolic pressures >95 mmHg, systolic pressures >150 mmHg, or signs of hypertensive end-organ damage.

Medication choices = Oral methyldopa and labetalol.

Preeclampsia Definition = New onset of hypertension

and proteinuria after 20 weeks gestation. Systolic blood pressure ≥140 mmHg OR

diastolic blood pressure ≥90 mmHg Proteinuria of 0.3 g or greater in a 24-hour

urine specimen Preeclampsia before 20 weeks, think MOLAR

PREGNANCY! Categories

Mild Preeclampsia Severe Preeclampsia

Eclampsia Occurrence of generalized convulsion and/or

coma in the setting of preeclampsia, with no other neurological condition.

Preeclampsia Severe Preeclampsia must have one of the

following: Symptoms of central nervous system dysfunction =

Blurred vision, scotomata, altered mental status, severe headache

Symptoms of liver capsule distention = Right upper quadrant or epigastric pain

Nausea, vomiting Hepatocellular injury = Serum transaminase

concentration at least twice normal Systolic blood pressure ≥160 mm Hg or diastolic ≥110

mm Hg on two occasions at least six hours apart Thrombocytopenia = <100,000 platelets per cubic

milimeter Proteinuria = 5 or more grams in 24 hours Oliguria = <500 mL in 24 hours Severe fetal growth restriction Pulmonary edema or cyanosis Cerebrovascular accident

Preeclampsia superimposed on Chronic Hypertension Affects 10-25% of patients with

chronic HTN Preexisting Hypertension with the

following additional signs/symptoms: New onset proteinuria Hypertension and proteinuria beginning

prior to 20 weeks of gestation. A sudden increase in blood pressure. Thrombocytopenia. Elevated aminotransferases.

Treatment of Preeclampsia

Definitive Treatment = Delivery Major indication for antihypertensive

therapy is prevention of stroke. Diastolic pressure ≥105-110 mmHg or

systolic pressure ≥160 mmHg Choice of drug therapy:

Acute – IV labetalol, IV hydralazine, SR Nifedipine

Long-term – Oral methyldopa or labetalol

Gestational Hypertension

Mild hypertension without proteinuria or other signs of preeclampsia.

Develops in late pregnancy, after 20 weeks gestation.

Resolves by 12 weeks postpartum. Can progress onto preeclampsia.

Often when hypertension develops <30 weeks gestation.

Indications for and choice of antihypertensive therapy are the same as for women with preeclampsia.

Risk Factors for Hypertension in Pregnancy Nulliparity Preeclampsia in a previous pregnancy Age >40 years or <18 years Family history of pregnancy-induced hypertension Chronic hypertension Chronic renal disease Antiphospholipid antibody syndrome or inherited

thrombophilia Vascular or connective tissue disease Diabetes mellitus (pregestational and gestational) Multifetal gestation High body mass index Male partner whose previous partner had preeclampsia Hydrops fetalis Unexplained fetal growth restriction

Evaluation of Hypertension in Pregnancy History

ID and Complaint HPI (S/S of

Preeclampsia) Past Medical Hx, Past

Family Hx Past Obstetrical Hx,

Past Gyne Hx Social Hx Medications, Allergies Prenatal serology,

blood work Assess for

Hypertension in Pregnancy risk factors

Physical Vitals HEENT = Vision Cardiovascular Respiratory Abdominal =

Epigastric pain, RUQ pain

Neuromuscular and Extremities = Reflex, Clonus, Edema

Fetus = Leopold’s, FM, NST

Evaluation of Hypertension in Pregnancy

Laboratory Tests CBC (Hgb, Plts) Renal Function (Cr, UA, Albumin) Liver Function (AST, ALT, ALP, LD) Coagulation (PT, PTT, INR, Fibrinogen) Urine Protein (Dipstick, 24 hour)

Management of Hypertension in Pregnancy Depends on severity of hypertension

and gestational age!!!!

Observational Management Restricted activity Close Maternal and Fetal Monitoring

BP Monitoring S/S of preeclampsia Fetal growth and well being (NST, and U/S)

Routine weekly or biweekly blood work

Management of Hypertension in Pregnancy

Medical Management Acute Therapy = IV Labetalol, IV Hydralazine,

SR Nifedipine Expectant Therapy = Oral Labetalol,

Methyldopa, Nifedipine Eclampsia prevention = MgSO4

Contraindicated antihypertensive drugs

ACE inhibitors Angiotensin receptor antagonists

Management of Hypertension in Pregnancy

Proceed with Delivery Vaginal Delivery VS Cesarean Section Depends on severity of hypertension! May need to administer antenatal

corticosteroids depending on gestation!

Only cure is DELIVERY!!!

•Prediction:Routine urine analysis•Prevention:Chocolate

Outline

IntroductionPredictionPrevention

Cochrane Systematic ReviewGold Standard' for high-quality systematic reviews

•Preeclampsia: Hypertension associated with proteinuria.

•Pathogenesis: • unknown (Barton& Sibai, 2008).

Impaired trophoblast differentiation& invasion

Placental & endothelial dysfunction Immune maladaptation to paternal Ags

Exaggerated systemic inflam response.

•Pathogenesis: • Differs with various risk factors: PG Vs MG with previous PEpreexisting vas dispreexisting DM or multifetal gestation.

In PE: Impaired trophoblast differentiation & invasion

Placental and endothelial dysfunction

PREDICTION OF PE

• Why prediction is important?• The ideal screening test • Methods I. Preconception factors II. Pregnancy-Related Factors 1. Risk factors 2. Markers

Why prediction is important:1.The risk for recurrent PE

can be as high as 65% (Barton&

Sibai, 2008).

2.PE is associated with substantial maternal& perinatal complications

The ideal Screening test: SimpleNoninvasiveRapidInexpensiveEasy to perform early in pregnancyHighly sensitivity & predictive.

I. Preconception factors1st step in the management of a woman with a history of PE is to conduct a detailed evaluation of potential risk factors (Barton& Sibai, 2008).

Preconceptional Risk FactorsRates of preeclampsia depend on: severity of underlying

complications & combinations of risk

factors . Risk% Risk factors

15-40 Chronic hypertension/renal disease

10-35 Pre gestational DM

10-20 Connective tissue disease (lupus, rheumatoid arthritis)

10-40 Thrombophilia (acquired or congenital) 10-15 Obesity/insulin resistance 10-20 Age older than 40 y

10-35 Limited sperm exposure

10-15 Family history of preeclampsia/ cardiovascular disease

1.5 fold Woman born as SFGA

2-3 fold

Adverse outcome in a previous pregnancy: IUGR, ab placentae, IUFD

II. Pregnancy-Related FactorsRegular antenatal care is mandatory for the prevention & early detection of PE .

Risk factors: Magnitude of risk depends on the number of factors

Hydrops/hydropic degeneration of the placenta

Multifetal gestationUnexplained FGRGestational hypertensionUTIPeriodontal infectionMarkersBiophysicalBiochemical

Markers Many Based on: pathophysiological abnormalities

•SCREENING TESTS FOR PE (WHO, 2004)

I. Placental perfusion & vascular resistance dysfunctionMean arterial blood pressureRoll over test Doppler ultrasound Isometric exercise test Intravenous infusion of angiotensin II Platelet angiotensin II binding Platelet calcium response to arginine vasopressin Renin 24-hour ambulatory blood pressure monitoring

II. Fetoplacental unit dysfunctionHuman chorionic gonadotropin Alpha fetoprotein Estriol Inhibin A Pregnancy-associated plasma protein A Activin A Corticotropin release hormone

III. Renal dysfunction Serum uric acid Microalbuminuria Urinary calcium excretion Urinary kallikrein Microtransferrinuria N-acetyl- glucosarninidase

Platelet countPlatelet activation and endothelial cell adhesion moleculesProstacyclinCytokinesIsoprostanes, Antiphospholipid antibodies, Placenta growth factorHematocritAntithrombin IllCalciumTransferrinAtrial natriuretic peptide

Fibronectin Endothelin Thromboxane Homocysteine Serum lipids Insulin resistance Plasminogen activator inhibitor Leptin Total proteins Magnesium Ferritin Haptoglobin microglobulin Genetic markers

IV. Endothelial& oxidant stress dysfunction

I. Biophysical• Mean arterial pressure• (2D BP+S BP)/3• Better predictor of PE than S& D BP (BMJ

200817;336:111; Meta-analysis of 34 RCT)

2nd trimester MA BP ≥ 90 mm Hg had +ve LR 3.5 and –ve LR 0.46 • BP remains the cornerstone of early diagnosis

although it has limitations:measurement errors associated with sphygmomanometereffect of maternal posture on BP in pregnant women}.

•Repeated routine urinalysis throughout pregnancy NOT useful for predicting PE

(JAMA 2003: 12;289(10):1220)

Uterine artery Doppler ultrasound• }impaired trophoblastic invasion of the spiral

arteries: reduction in uteroplacental blood flow}• High pulsatility index and/or Notch in 1st & 2nd

trimesters: poor predictor of PE(Papgeorghiou & Leslie, 2007)

Uterine artery Doppler plus biochemical markers• Promising results • Current data do not support this combination for

routine screening for PE (Barton& Sibai, 2008).

Diastolic Notch in uterine artery waveform

The Roll over testNot of value in predicting PE

II. Biochemical Markers

Angiogenic factors before & after the onset of PE(Barton& Sibai, 2008).

Serum placental growth factor: reducedSoluble fms-like tyrosine kinase: elevatedEndoglin: elevated

Conclusion•BP remains the cornerstone of early diagnosis

•MarkersReliability is inconsistentMany suffer from poor specificity & predictive values.None provided a cutoff value that could be clinically useful for the prediction of PE (Widmer et al, 2007).

•Currently: There is no clinically useful screening test to predict PE (WHO, 2004)

PrimarySecondary

Prevention of PE

Primary prevention•Avoiding occurrence of the disease•Obese:achieve an ideal b wt before conception (Villamor& Cnattingius, 2006)

No RCT•Ch hypertension:Control BP before conception. No RCT

• Pregestational DM:-Complete her family as early as possible & before vascular complications develop -Control DM before conception & throughout pregnancy

Secondary• Breaking off the disease process before

emergence of obvious clinical disease• {Etiology of the disease is unknown} • To correct theoretical pathophysiology• I. Non pharmacologicalII. Nutritional III. Pharmacological

I. Non pharmacological1. Daily Bed restRest for 4-6 h/dMay reduce risk of PE for women with normal BP (level 2 evidence) (Cochrane Library 2006 Issue 2:CD005939)

2. Life-style changes •High job stress: greater risk of PE(Sharma& Mittal, 2006)

•Reducing job stress may be beneficial in the prevention of PE

3. Regular prenatal exercise• May prevent or oppose progression (Weissgerber et al, 2004)

• {Stimulation of placental growthReduction of oxidative stressReversal of maternal endothelial dysfunction}. • Insufficient evidenceModerate intensity regular aerobic exercise(Cochrane Library 2006 Issue 2:CD005942) Aerobic exercise =cardiovascular exercise=any sustained rhythmic activity that involves large muscle groups: makes the lungs work harder as the body's need for oxygen is increased.

• Stretching exercises are more effective at reducing the risk of PE than walking

(University of North Carolina,2008)

Smoking: Reduced risk for PE (Sibai et al, 2005).

{Nicotine inhibition of interleukin-2 & tumor necrosis factorEffects of nicotine on angiogenic proteins}. Smoking: abnormal fetal growthpreterm birthAbruptionAdverse effects on maternal health.

II. Nutritional1. Higher total dietary fiber intake in early pregnancy may reduce risk for PE(level 2 evidence) Prospective cohort study Am J Hypertens 2008 Aug;21(8):903

2. Increasing dietary protein & energy intake RCT: no benefit

• 5 or more servings of chocolate/w in 3rd trimester:40% reduction

(Triche, 2008; Epidemiology .19:459-464), Yale University

{Chocolate, especially dark chocolate, is rich in theobromine: stimulates the heart, relaxes smooth muscle & dilates blood vessels, and has been used to treat chest pain, high blood pressure}

3 .Garlic Insufficient evidence to recommend for preventing PE

2006 3: 006Cochrane Library Issue CD065

)

4. Dietary sodium restriction • No significant differences (Cochrane Library 2005 Issue 4:CD005548)

6. Fish Oil Supplementation • Observational studies: beneficial effects • {inhibition of platelet thromboxane A2 without affecting

prostacyclin: shifting the balance toward a reduced platelet aggregation and increased VD}.

• RCT: No benefit (Olsen et al, 2000)

• High doses: increase the risk of PIH(Olafasdottir et al, 2006).

• Not recommended for the prevention of PE

5. Weight Reduction •Although obesity is a known risk factor, there is no evidence that limiting wt gain during pregnancy; reduces its occurrence.

• Wt reduction is not recommended during pregnancy even in obese women (Kramer, 2004)

III. Pharmacological

1 .Low-dose Aspirin • {inhibits biosynthesis of platelet thromboxane A2

with little effect on vascular prostacyclin production: altering the balance in favor of prostacyclin}.

• (50-150 mg/day) For women with a previous history of hypertension or PE (n=6,107):Small to moderate benefits, safe. level 2 evidence (Cochrane Library 2007 Issue 2:CD004659)

2. Low-dose Aspirin/Heparin•History of severe preterm PE & LBW infants.

(Sergio et al, 2006)

•Lower incidence of PE (3Vs 30%)

Greater gestational age at deliveryHigher birth wt

3. Calcium Supplementation • Reduces the risk of PIH, particularly in populations that have diets deficient in calcium

level 1 evidence (Cochrane Syt review , 2006)

• The relationship between cal & risk of PIH is inconsistent& inconclusive

The relationship between cal & the risk of PE is highly unlikely.Evidence-based review by FDA (2007)

4. Antihypertensive Drugs •Mild to moderate hypertension: Halving in the risk of developing severe hypertensionNo difference in the risk of developing PE or proteinuria (Cochrane syst review, 2007)

5. Diuretics •No reduction in the incidence of PE or perinatal mortality

•May have deleterious effects: reduced renal & placental perfusion. (Cochrane Library 2007 Issue 1:CD004451)

6 .Antioxidant supplementation may not affect risk of PE or clinical outcomes

2 level evidence

( 2008 Cochrane Library Issue 1: 004227CD)

7 .Concomitant Vit C& E supplementation • {PET: imbalance of oxidant & antioxidant activity:

multiorgan endothelial dysfunction}. • Vit C (1,000 mg/d) plus vit E (400 IU/ d)• Did not prevent PElevel 2 evidence (Obstet Gynecol 2007 Dec;110(6):1311)• May increases rate of LBW infants& might be associated with higher rate of SB

level 2 evidence (Lancet 2006 Apr 8;367(9517):1145

8. Magnesium •{Mg is beneficial for the prevention & tt of severe PE & E

Decreased intracellular Mg in PE} •No effect•(365 mg& 500 mg).Cochrane syst review, 2004

9. Folic acid& other B-vits •{Deficiency of vit B2 may cause biochemical changes simulating abnormalities of PE}

•No evidence that any of B vits can prevent PE

(Shrama& Mittal, 2006).

10. Zinc supplementation • {Zinc concentrations are reduced in PE}

•RCT: No benefit(Jonsson et al, 1996)

11. Nitric oxide Insufficient evidence for preventing PECochrane Library 2007 Issue 2:CD006490

12. Progesterone Insufficient evidence for preventing PE Cochrane review, 2006

ConclusionRegular antenatal care is mandatory for the prevention & early detection of PE. For prevention of PEBed restReduction of job stressHigh dietary fiber intake Low dose aspirinLow dose aspirin/heparinCa supplementation

PREECLAMPSIA

PREECLAMPSIA

Hypertensive disorder specific to pregnancy affects nearly 6% of all pregnancies a major cause of maternal and neonatal

mortality and morbidity 15 to 20 % of maternal mortality in

developed countries

PREECLAMPSIA

Severity ranges from: a mild disorder (transient hypertension

in the later part of the pregnancy) to a life-threatening disorder with seizures,

HELLP syndrome, fetal hypoxia, and growth retardation

more severe disease: 0.56 per 1000 deliveries

PREECLAMPSIA

Predisposes women to other serious complications: placental abruption acute renal failure cerebral hemorrhage disseminated intravascular coagulation circulatory collapse

PREECLAMPSIA

The etiology is unknown believed to be involved:

immune maladaptation placental ischemia oxidative stress genetic susceptibility

PREECLAMPSIA

Classification of hypertension in pregnancy Gestational hypertension Preeclampsia / eclampsia Chronic hypertension Preeclampsia superimposed on chronic

hypertension

PREECLAMPSIA

Definition of hypertension a systolic blood pressure of 140 mmHg

or above, or a diastolic blood pressure of 90mmHg

or above, on two occasions 6 hours apart

Abnormal proteinuria the excretion of 300 mg or more of

protein in 24 hours

PREECLAMPSIA

Criteria for severe preeclampsia Blood pressure: > 160 mmHg systolic or

> 110 mm Hg diastolic Proteinuria: > 5 g in 24 hours Persistent and severe cerebral or visual

disturbances (headache, scotoma, blurred vision)

Persistent and severe epigastric pain or right upper quadrant pain

PREECLAMPSIA

Criteria for severe preeclampsia Pulmonary edema or cyanosis Oliguria (< 500 mL of urine in 24 hours) Eclampsia (grand mal seizures) HELLP syndrome

PREECLAMPSIA

Screening tests for gestational hypertension

routine components of antepartum care trimester

early detection of vasoconstriction early detection of altered renal function early detection of altered hemodynamics detection of placental hypoperfusion /

ischemia detection of endothelial activation or

injury detection of an activated coagulation /

fibrinolytic system

PREECLAMPSIA

Prevention of preeclampsia women at risk: multifetal gestation,

vascular or renal disease, previous severe preeclampsia-eclampsia, abnormal uterine artery Doppler velocimetry

antihypertensive drugs magnesium zinc fish oil calcium low-dose aspirin

PREECLAMPSIA

Mild preeclampsia - management < 37 weeks gestation

inpatient or outpatient management worsening disease: delivery, magnesium

sulfate > 40 weeks gestation

delivery, magnesium sulfate 37 - 39 weeks gestation

inducible cervix: delivery, magnesium sulfate

cervix not inducible: inpatient or outpatient management

PREECLAMPSIA

Severe preeclampsia - expectant management gestational age: not recommended for <

24 weeks or > 34 weeks gestation hospitalization: tertiary care center antenatal testing: daily

PREECLAMPSIA

Severe preeclampsia - guidelines for expedient delivery maternal indications

eclampsia, thrombocytopenia, pulmonary edema, acute renal failure

persistent severe headache or visual changes

elevated liver enzymes with persistent severe epigastric pain or right upper quadrant tenderness

labor or rupture of membranes vaginal bleeding, abruptio placenta

PREECLAMPSIA

Severe preeclampsia - guidelines for expedient delivery fetal indications

repetitive severe variables or late decelerations

biophysical profile < 4 on two occasions 4 hours apart

amniotic fluid index < 2 cm intrauterine growth restriction fetal death > 34 weeks gestation

PREECLAMPSIA

Severe preeclampsia - management protocol admission to labor and delivery for 24

hours magnesium sulfate IV for 24 hours antihypertensives if diastolic blood

pressure > 110 mmHg meet guidelines for expedited delivery?

yes? delivery

PREECLAMPSIA

Severe preeclampsia - management protocol Expedited delivery? no?

< 23 weeks: counseling for termination of pregnancy

23-32 weeks: steroids, antihypertensive medications, daily maternal and fetal evaluation, delivery at 34 weeks

32-33 weeks: amniocentesis immature fluid - steroids, delivery in 48

hours

PREECLAMPSIA

HELLP syndrome - diagnosis 10% before 27 weeks 20% after 37 weeks 70% between 27 and 37 weeks slow initial phase with accelerated final

phase versus secondary expression of sepsis, ARDS, renal failure

PREECLAMPSIA

HELLP syndrome parameters used to diagnose

preeclampsia are not reflective of disease severity

target organ systems liver brain kidneys coagulation system

increased maternal and perinatal risk

PREECLAMPSIA

HELLP syndrome - diagnostic criteria hemolysis

abnormal peripheral smear lactate dehydrogenase > 600 U/L

elevated liver enzymes serum aspartate aminotransferase > 70

U/L lactate dehydrogenase > 600 U/L

low platelets platelet count < 100,000/mm3

PREECLAMPSIA

HELLP syndrome - differential diagnosis acute fatty liver of pregnancy appendicitis diabetes insipidus gallbladder disease gastroenteritis glomerulonephritis hemolytic uremic syndrome hepatic encephalopathy

PREECLAMPSIA

HELLP syndrome - differential diagnosis idiopathic thrombocytopenia kidney stones pancreatitis pyelonephritis systemic lupus erythematosus thrombotic thrombocytopenia purpura viral hepatitis

PREECLAMPSIA

HELLP syndrome - antepartum management

assess and stabilize the maternal condition

correct coagulopathy if DIC is present give intravenous magnesium sulfate to

prevent seizures provide treatment for severe hypertension

to prevent stroke transfer to tertiary center if appropriate if subcapsular hematoma of liver,

computed tomography or ultrasound of the abdomen

PREECLAMPSIA

HELLP syndrome - antepartum management evaluate fetal well-being

non stress test biophysical profile

timing of delivery if > 34 weeks gestation, deliver if < 34 weeks gestation, administer

corticosteroids, then deliver in 48 hours

PREECLAMPSIA

HELLP syndrome - management for cesarean birth use general anesthesia if platelet count

is < 75,000 / mm3

transfuse 5 to 10 units of platelets before surgery if platelet count is < 50,000 / mm3

leave vesicouterine peritoneum open install subfascial drain

PREECLAMPSIA

HELLP syndrome - management for cesarean birth schedule secondary closure of skin

incision or subcutaneous drain administer postoperative transfusions as

needed perform intensive monitoring for at least

48 hours postpartum consider dexamethasone (10 mg IV

every 12 hours) until postpartum resolution of disease occurs

PREECLAMPSIA

HELLP syndrome - management of women with a subcapsular liver hematoma general considerations - blood bank

aware for potential need of many units of blood

general or vascular surgeon consultation avoid direct and indirect manipulation of

liver closely monitor hemodynamic status management of hematoma depends on

whether it is ruptured or not

PREECLAMPSIA

Eclampsia occurrence of convulsions or coma

unrelated to other associated conditions all new onset seizures during pregnancy

- eclampsia until proven otherwise incidence: 1 in 500 pregnancies

3% in multiple gestations

PREECLAMPSIA

Eclampsia precise cause unknown theories

vasospasm ischemia edema multisystem organ failure

PREECLAMPSIA

Eclampsia seizures usually occur without aura hypertension not severe in 20% edema absent in 30% proteinuria absent in 20% hyperreflexia is not predictive of seizure headache or visual changes - most

common precipitating event

PREECLAMPSIA

Eclampsia 80% of convulsions occur before or

during the delivery 1/3 of cases may be not preventable atypical

less than 20 weeks gestation more than 48 hours postpartum

PREECLAMPSIA

Eclampsia - risk factors low socioeconomic status extremes in childbearing age African-American no prenatal care substance abuse

PREECLAMPSIA

Eclampsia - management control convulsions correction of hypoxia and acidosis blood pressure control delivery after maternal stabilization

PREECLAMPSIA

Eclampsia - anticonvulsant therapy magnesium sulfate

mechanism of action - smooth muscle relaxation by displacement of calcium

dosage - 4-6 g intravenous loading dose, followed by 2 g per hour

may be given intramuscularly

PREECLAMPSIA

Eclampsia - magnesium sulfate side effects:

maternal hypotonia respiratory depression cardiac arrest neonatal depression

contraindicated in myasthenia gravis use with caution in renal insufficiency

PREECLAMPSIA

Eclampsia - anticonvulsant therapy phenytoin

used extensively in Europe may be used in myasthenia gravis mechanism of action - may increase

gamma aminobutyric acid-mediated chloride conduction in postsynaptic membranes

may inhibit neurotransmitter inhibitory systems

PREECLAMPSIA

Eclampsia - phenytoin dosage - 1 g loading dose over 1 hour cardiac monitoring during administration side effects

arrhythmias with rapid administration hepatitis Steven-Johnson syndrome

PREECLAMPSIA

Eclampsia - anticonvulsant therapy diazepam

useful for status seizures mechanism of action - facilitate the

binding of GABA to its receptor benzodiazepine receptors

dosage - 10 mg at a rate of 5 mg per min may be repeated at 10 to 15 minute

intervals

PREECLAMPSIA

Eclampsia - diazepam side effects - loss of consciousness,

hypotension, respiratory depression caution - may increase risk of aspiration causes prolonged depression of the

neonate sodium thiopentotal

long acting barbiturate used when sedation, paralysis and

intubation needed

PREECLAMPSIA

Eclampsia - which anticonvulsant to use? magnesium is associated with

decreased recurrence risks of seizures when compared with diazepam or phenytoin

diazepam is associated with increased need for mechanical ventilation

PREECLAMPSIA

Eclampsia - management of fetus fetal bradycardia during seizure

~ 5 minutes after the onset of the seizure may be associated with rebound

tachycardia recovery phase may show late

decelerations monitor for uterine hypertonicity

allow for fetal recovery monitor for signs of abruption

PREECLAMPSIA

Eclampsia delivery is indicated regardless of

gestational age immediate cesarean delivery is not

necessary

PREECLAMPSIA

Eclampsia - radiographic evaluation should be reserved for women with

neurological deficit, recurrent seizures, or atypical presentation

abnormal CT findings - 50% edema, hemorrhage, infarction

cerebral angiography has limited use 90% of EEG evaluations may be

abnormal

PREECLAMPSIA

Eclampsia - management allow patient to have seizure use bite block as needed to prevent

maternal injury establish airway administer magnesium sulfate as soon as

possible obtain arterial blood gases monitor urine output control hypertension

PREECLAMPSIA

Eclampsia - management rebolus with magnesium sulfate if repeat

seizure occurs do not intervene for fetal status while

mother is unstable if seizure continues, paralyze and

intubate.

PREECLAMPSIA

Counseling regarding future pregnancies - HELLP syndrome information available varies recurrent risk of preeclampsia: 43%

(19%) recurrent risk of HELLP syndrome: 19-

27% (3%) If HELLP syndrome < 32 weeks

recurrent risk of preeclampsia / eclampsia is 61%